| First Author | Chen J | Year | 2004 |
| Journal | Biochem Biophys Res Commun | Volume | 318 |
| Issue | 1 | Pages | 88-94 |
| PubMed ID | 15110757 | Mgi Jnum | J:89356 |
| Mgi Id | MGI:3039979 | Doi | 10.1016/j.bbrc.2004.03.187 |
| Citation | Chen J, et al. (2004) Heme oxygenase-2 gene deletion increases astrocyte vulnerability to hemin. Biochem Biophys Res Commun 318(1):88-94 |
| abstractText | In a prior study, we observed that heme oxygenase-2 gene deletion protected murine cortical neurons from heme-mediated injury. In the course of these studies, constitutive HO-2 expression was observed in astrocyte cultures. The present study tested the hypothesis that astrocytes lacking the HO-2 gene would be less vulnerable to heme. Contrary to this hypothesis, gene deletion resulted in a 50-75% increase in cell death after 6h exposure to 30 or 60microM hemin, as measured by LDH release. A similar effect was observed when cell viability was assessed with the MTT assay. HO-2 gene deletion did not alter cellular expression of HO-1. The increased sensitivity of knockout astrocytes to hemin was reversed by increasing HO-1 expression by adenoviral gene transfer. These results suggest that heme oxygenase protects astrocytes from heme-mediated oxidative injury and highlight the disparate effect of HO in neurons and astrocytes. |
